NSAIDs can increase BP (though effect varies widely) -- take in smallest dose for least amount of time. If on antihypertensive/diuretic and become uncontrolled, consider switch to CCB (least affected by NSAIDs).

fast onset (begin working within one "arm to brain" circulation time). however, vessel-rich organs also quickly uptake drugs reducing their levels in the blood (and therefore the brain) in a matter of minutes. therefore, termination action of single bolus is more the result of redistribution than metabolism/elimination.

degree of paralysis can be measured with nerve stimulator -- partial = small twitch c TOF fade, compete = no contraction. zero contractions with train of four test will not respond to reversal medication, will only cause side effects (bradycardia, salivation/mucous, bronchospasm, N/V/D, urination -- also OD causes paradoxical reparalyzes!)

Chronic alcoholism -> increased 2E1 activity -> faster generation of NAPQI. Low GSH stores due to young age or malnutrition. Reduced liver conjugation leaving more to be metabolized by 2E1.

opioids MOA

bind to opioid receptors (G-protein coupled) located in the brain and spinal cord. The main opioid receptor is the Mu receptor, of which there is over 100 polymorphisms (variation in response! -- may also be incomplete cross tolerance between opioids)